With the intensification of population aging and the popularity of electronic products, the incidence of retinal diseases continues to rise, and their complex pathogenesis seriously restricts the development of effective treatment strategies. Zebrafish has become an important model animal for ophthalmic research, especially for retinal disease research, due to its unique biological advantages. This article aims to systematically review the current application status and prospects of zebrafish models in various retinal disease research, broaden future research ideas, and provide new perspectives for the prevention and treatment of retinal diseases. This article first elaborates on the unique advantages of zebrafish as a model animal, including easy feeding, transparent embryos, rapid development of the visual system, high homology with human genes, and strong retinal regeneration ability. Subsequently, we reviewed the research and application progress of zebrafish models, focusing on various hereditary and non-hereditary retinal diseases, including diabetic retinopathy, retinopathy of prematurity, retinitis pigmentosa, rod-cone cell dystrophy, Leber congenital amaurosis, congenital static night blindness, choroidal deletion, and Budd Beeder syndrome. Studies have confirmed that a large number of zebrafish models simulating the pathological characteristics of human retinal diseases have been constructed successfully using genetic techniques such as CRISPR/Cas9 gene editing, TALEN targeted modification, chemical induction, and microinjection. These models not only effectively reproduce the clinical phenotype of retinal diseases but also play an irreplaceable role in elucidating the functions of pathogenic genes, revealing signal pathway disorders, and analyzing the mechanisms of cell death and regeneration. Additionally, the zebrafish model has shown great potential in drug screening and efficacy evaluation. These studies indicate that the zebrafish model is an ideal tool for in-depth analysis of the pathogenesis of retinal diseases, promoting precision medicine and new drug development, and has broad application prospects in the future.
ObjectiveTo investigate relationship between ultrastructural changes and expression of basic fibroblast growth factor of diabetic retinopathy in rats.MethodsDiabetes was induced in rats with a single injection of streptozotocin (STZ) and divided into normal control group and 1- , 3- and 5- month diabetes group. The paraffin slide was observed by in-situ hybridization and immunohistochemistry, and retinal ultrastructure was examined by transmission electron microscopy.ResultsNo change of retinal ultrastructure was found in the control group. Different degrees of ultrastructure lesion were found in 1-month diabetic rats with fragmental increase of thickness of basement membrane, swelling of endothelial cells and obvions fingerlike processes in the capillary cavity, disconcentration of heterochromatin both in endothelium and pericyte, and swelling and degeneration of mitochondrion. The edema of endothelial cells of 3-month diabetic rats was more serious than that of 1month ones, and the capillary cavity was nearly occluded. In 5-month diabetic rats, the basement membrane was unevenly thickened, or obviously split. The positive rate of in-situ hybridization in 3-month diabetic rats was 77.8% while the positive rate of immunohistochemical stain was 55.6%, which increased to 88.9% in 5-month diabetic rats.ConclusionsThe occurrence of the ultrastructural changes in STZ rats with diabetic retinopathy is earlier than that of the expression of bFGF.(Chin J Ocul Fundus Dis, 2003,19:348-351)